Common genetic variation safeguards children from asthma

Genetic protection for lung inflammation vanishes when children constantly breathe in high-traffic pollution

Gas, diesel exhaust, brake wear metals or resuspended road dust could all contribute to children’s poor respiratory health, according to the USC study. (Photo/Library of Congress)

Too much residential traffic removes the protective effect a specific gene has on lowering asthma risk, according to a new USC study.

Children could have zero, one or two copies of a common gene variant.

“Environmental exposures such as traffic-related air pollution can trigger lung inflammation, but the effects depend on genetic background,” said Frank Gilliland, senior author, preventive medicine professor and director of the Division of Environmental Health at the Keck School of Medicine of USC. “Some people have a genetic background that reduces their risk for lung inflammation, but if they are highly exposed, then that protection goes away.”

The study, published Dec. 29 in the journal PLOS One, examined exhaled nitric oxide levels in 2,457 white and Hispanic children in Southern California.

Airway inflammation

Exhaled nitric oxide is a biomarker of airway inflammation; higher levels of it increase a child’s risk of developing asthma. Children with a common variation of “NOS2,” the primary gene that produces nitric oxide in airways, tend to have lungs that are less inflamed. Thus, they are less likely to develop asthma.

Towhid Salam, lead author and assistant professor of research at Keck Medicine of USC, said the gene variant is fairly common. About one in three whites and Hispanics have it in their genetics, he said.

Some 6.8 million children in the United States have asthma, according to the Centers for Disease Control and Prevention. Children in poor families were more likely to have been diagnosed with asthma than children in more well-to-do families, according to the 2012 National Health Interview Study.

“Scientists have a lot of uncertainty about children’s exposure to fresh tailpipe emissions from cars around their homes and schools,” Salam said. “The Environmental Protection Agency does not require the measurement of car exhaust in residential areas, but traffic count data is maintained for freeways and major streets.”

Gasoline, diesel exhaust, brake wear metals or resuspended road dust could all contribute to children’s poor respiratory health, according to the study.

The next step in this research is to take direct measurements closer to home and to have better data of the air pollution cocktail in vehicular traffic that residential streets create, Gilliland said.